A new approach to the question of the regulation of gene expression in higher cells is suggested by our discovery that has established the existence of a new control-mechanism operating late after infection in cells productively infected with SV40 as well as in the mitochondria in HeLa cells. This control operates during symmetrical transcription of the DNA, and it determines the stability of the primary gene products and the portion of each RNA molecule ultimately exported to the cytoplasm. The overall objectives of this project has been a) To extend the observation of symmetrical transcription to other DNA tumor viruses; (recently, symmetrical transcription mechanism has been confirmed for polyoma and has also been demonstrated in Adeno and Herpes virus infected cells). b) To determine the mechanism SV40 transcription early in the infection and in transformed cells. c) To determine the mechanism of symmetrical transcription from SV40 DNA/or polyoma DNA in lytically infected cells. d) To determine the subcellular fraction where the processing of the viral RNA takes palce. e) To determine the mechanism for selective degradation of particular RNA sequences. f) To determine whether "normal" genes are transcribed symmetrically.